Mutation spectrum and genotype-phenotype correlation was analyzed in patients with familial hypercholesterolemia in Chinese population.

Given that overexpression of these LOF PCSK9 variants does not cause UPR activation under normal homeostatic conditions, therapeutic strategies aimed at blocking the autocatalytic cleavage of PCSK9 in the ER represent a viable strategy for reducing circulating PCSK9

PCSK9 was inconsistently associated with cardiovascular (CV) events in populations with type 2 diabetes. The association may depend on the level of CV risk and the background treatment.

These findings support a model in which SURF4 functions as an endoplasmic reticulum cargo receptor mediating the efficient cellular secretion of PCSK9.

A long-term physical activity caused increase in PCSK9 blood levels.

The present study shows that serum PCSK9 levels, but not PCSK9 polymorphisms, are associated with coronary artery disease risk in Southern Chinese Han population, and that serum PCSK9 levels are positively associated with AIP

In Japanese male subjects, the concentrations of serum PCSK9 and TBIL were correlated with periodontal parameters.

C679X loss-of-function PCSK9 variant lowers fasting glucose levels.

There was no protective or no deleterious effect of carrying PCSK9 LOF mutations on AD [Alzheimer disease]prevalence nor on age of onset, even when stratified by apolipoprotein E epsilon 4 genotype or by gender. Conclusion: Our data indicate that carrying PCSK9 LOF mutations has a neutral effect on neurocognitive health and the prevalence of AD [Alzheimer disease].

Taken together, the present study provides evidence of a pro-inflammatory action of PCSK9 on macrophages, mainly dependent by the LDLR.

HepG2 cell lines transfected with siRNA directed to PCSK9 were challenged with Hcy, homocysteine thiolactone (HTL), testosterone, 5alpha-dihydroxytestosterone (5alpha-DHT), or estradiol for 24h, leading to an overt expression of PCSK9 and down-regulated expression of LDLR.

Given that overexpression of these LOF PCSK9 variants does not cause UPR activation under normal homeostatic conditions, therapeutic strategies aimed at blocking the autocatalytic cleavage of PCSK9 in the ER represent a viable strategy for reducing circulating PCSK9

Data suggest that expression of Pcsk9 and Ldlr in liver and pancreas can be regulated by dietary measures; here, dietary supplementation with quercetin-3-glucoside modulates expression of Pcsk9 and Ldlr in prevention of hyperlipidemia and hyperinsulinemia induced by high dietary cholesterol. (Pcsk9 = proprotein convertase subtilisin/kexin type-9; Ldlr = low-density lipoprotein receptor)

The data of the present study demonstrated that the PCSK9 shRNAmediated antiapoptotic effect induced by MCAO in hyperlipidemic mice is associated with ApoER2 downregulation, which may be a potential new therapy for stroke treatment in patients with hyperlipidemia.

It was concluded that quercetin inhibits oxLDLinduced lipid droplets in RAW264.7 cells by upregulation of ABCAl, ABCG1, LXRalpha and downregulation of PCSK9, p53, p21 and p16.

PCSK9 overexpression in the aorta may promote acute aortic dissection.

The present study aimed to explore the direct toxicity of proprotein convertase subtilisin/kexin type 9 (PCSK9) to atherosclerosis (AS) and its association with apoptotic endothelial cells.

present anti-PCSK9 vaccine induced long-lasting anti-PCSK9 antibody production and improved lipoprotein profiles. Thus, anti-PCSK9 vaccine could become a new option for the treatment of dyslipidemia as a long-acting therapy in future

PCSK9 may act as an inflammatory mediator in the pathogenesis of atherosclerosis via TLR4/NF-kappaB signaling pathway.

PCSK9, by sustaining smooth muscle cell synthetic phenotype, proliferation, and migration, may play a pro-atherogenic role in the arterial wall

PCSK9 inhibits lipoprotein(a) clearance through the LDLR.

Use Crispr-Cas system to introduce nonsense variants into PCSK9 to lower blood cholesterol levels.

Studied the combination model of a single AAV-PCSK9 injection, high-fat diet, and partial carotid ligation which induces robust atherosclerosis in the flow-disturbed carotid artery within 3 weeks in C57 mice, and results suggest this is a quick and convenient model to study atherosclerosis and mechanisms using any knockout or transgenic mice without having to generate double knockouts.

These observations suggest positive feedback interplay between SMC-derived PCSK9 and mtDNA damage in the proinflammatory milieu involving mtROS. This interaction results in cellular injury, characterized by apoptosis-a hallmark of atherosclerosis.

the PCSK9-gain-of-function mutation induces rapid development of atherosclerosis in peripheral vessels of Ossabaw pigs, which is exacerbated by a high-cholesterol diet.

PCSK9 Protein Überblick

Protein Überblick

This gene encodes a proprotein convertase belonging to the proteinase K subfamily of the secretory subtilase family. The encoded protein is synthesized as a soluble zymogen that undergoes autocatalytic intramolecular processing in the endoplasmic reticulum. The protein may function as a proprotein convertase. This protein plays a role in cholesterol homeostasis and may have a role in the differentiation of cortical neurons. Mutations in this gene have been associated with a third form of autosomal dominant familial hypercholesterolemia (HCHOLA3).